索拉菲尼对人胃癌细胞SGC-7901增殖、凋亡和P-ERK表达的影响

目的：探讨多分子靶向药物索拉菲尼（sorafenib）对体外人胃癌细胞SGC-7901增殖、凋亡的影响及对癌细胞P-ERK表达的影响，并探讨其可能机制。 方法：以MTT法检测索拉菲尼对SGC-7901细胞的杀伤抑制作用；免疫细胞化学法检测胃癌细胞内P-ERK蛋白的表达；流式细胞仪检测胃癌细胞凋亡的变化情况。 结果：索拉菲尼对胃癌细胞生长增殖具有抑制作用，随药物浓度的增加作用也增强，呈剂量—时间双效应关系(P<0.05)；经索拉菲尼处理的SGC-7901细胞的P-ERK表达明显下降(P<0.05)；细胞凋亡率增高(P<0.05)。 结论：sorafenib在体外对SGC-7901细胞具有明显的抑制作用，主要机制为抑制其P-ERK表达，从而抑制其增殖和促进凋亡。

The effect of sorafenib on growth| apoptosis and P-ERK expression in human gastric cancer SGC-7901 cells

Objective:To investigate the multiple molecular targeted agent, sorafenib, in human gastric cancer SGC-7901 cell proliferation, apoptosis and P-ERK expression, and explore its possible mechanism. Methods:MTT method was used to detect antiproliferative ratio of sorafenib on human gastric cancer SGC-7901 cell; immunocytochemical method for detection of gastric cancer cells P-ERK protein expression; and flow cytometry to analyze gastric cancer cell apoptosis. Results:Sorafenib obviously inhibited proliferation of gastric cancer cells and showed time-dose-dependent effects (P<0.05). When gastric cancer SGC-7901 cells were treated with sorafenib, immunocytochemistry showed that P-ERK expression was significantly decreased (P<0.05); flow cytometry showed that the SGC-7901 cell apoptosis rate increased (P<0.05). Conclusions:Sorafenib can significantly inhibit human gastric cancer SGC-7901 cell growth in vitro; the main mechanism is the inhibition of P-ERK expression, and thereby inhibit their proliferation and promote apoptosis.